Opiate receptor mediated inhibition of adenylate cyclase requires the presence of a GTP binding protein, Ni in order to be expressed. Pertussis toxin catalyzes the ADP-ribosylation of Ni and thereby attenuates the inhibitory actions of opiate, and other receptors on adenylate cyclase. Adenylate cyclase inhibition is accompanied, and probably caused by increased GTP hydrolysis which is also blocked by toxin treatment. A third role of Ni is in the control of opiate binding affinity and this too is lost on treatment with the toxin. Affinity labelling of opiate receptors with fentanylisothiocyanate (FIT) has led to the identification and partial purification of a 58,000 Mr glycoprotein subunit of the receptor. Active opiate receptors have been transferred from solution to liposomes as a first step in their reconstitution.